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钾离子去极化的大鼠尾动脉对肾上腺素和5-羟色胺的反应。

Responses of potassium-depolarized rat tail arteries to adrenaline and serotonin.

作者信息

Polidoro J H, Savino E A

出版信息

Arch Int Pharmacodyn Ther. 1987 Apr;286(2):206-11.

PMID:3592864
Abstract

Dose-response curves to adrenaline and serotonin were obtained from tail arteries incubated in standard, high potassium or low sodium media. The last one was used to test whether the effects of high potassium medium could be influenced by the concomitant lowering of the sodium concentration. The effects of endogenous catecholamines were eliminated by means of reserpine pretreatment, in vitro denervation with 6-OHDA or adrenergic blockade with phentolamine. Any of these procedures abolished the sustained contractile responses to high potassium, which then produced only small transient contractions. Dose-response curves to serotonin were not altered in the high potassium medium whereas those to adrenaline displayed slight changes. Inasmuch the responsiveness remained almost unchanged even though the effects of either agonist on the membrane potential had been virtually abolished, it was concluded that pharmacomechanical coupling is the major mechanism involved in the contractile responses of the tail artery.

摘要

从在标准、高钾或低钠培养基中孵育的尾动脉获得了对肾上腺素和5-羟色胺的剂量反应曲线。使用低钠培养基来测试高钾培养基的作用是否会受到伴随的钠浓度降低的影响。通过利血平预处理、用6-羟基多巴胺进行体外去神经支配或用酚妥拉明进行肾上腺素能阻滞来消除内源性儿茶酚胺的作用。这些程序中的任何一种都消除了对高钾的持续收缩反应,高钾随后仅产生微小的瞬时收缩。在高钾培养基中,对5-羟色胺的剂量反应曲线没有改变,而对肾上腺素的剂量反应曲线则有轻微变化。由于即使两种激动剂对膜电位的作用实际上已被消除,反应性仍几乎保持不变,因此得出结论,药物机械偶联是尾动脉收缩反应的主要机制。

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